Tag Archives: tapping test

To evaluate the effects of my medications, I use an app on my iPhone.
I don’t have the tremor that most people (including myself) associate with Parkinson’s, but instead I have bradykinesia (slowness of movement) and rigidity with a bit of balance and gait problems, just to make it more interesting.
I did know that tapping tests are used to evaluate Parkinson’s clinically so I looked for a tapping test on my iPhone and found “FastFingers”. The app has a window divided in two halves and I think that you are supposed to alternate the tapping between the two halves, but I only use one side. I make sure that the lower part of my palm, thumb, ring finger and little finger are resting against the table, see photo, and tap with my middle finger as fast as I can for 30 seconds. I do this with my right and my left hand a number of times throughout the day and record the results (time and number of taps).

I started collecting baseline data a number of weeks ago and actually found it more difficult than expected to capture enough data in a day to be able to find meaningful patterns. I was able to record enough data for two days, 12th and 13th March, and the results are plotted below with number of taps in 30 seconds on the y-axis and the time for the test on the x-axis. I also included a control, a.k.a. hubby

Thank you Zalamanda and Marten, for your comments on my previous post. Of course, I agree with both of you, two days is far too short a time to expect any kind of significant results. Nevertheless, I did observe some potentially interesting findings in these two days.

The first graph shows the measurements i did on my very first day on the new dose. And the small change I did was that I now take my second dose of the day, a “type A” medication (see a previous post here) at 11 am instead of 11:30 am and have also added a “type C” medication, that hopefully will make this dose last longer and if I’m lucky, the dose will have effect until dose number 3 at 3 pm so I don’t have to take that earlier.

Interestingly enough, the measurements of the very first day on the new dose, indicates that the small shift in time for dose number 2 actually has an effect. Both my right and my left hand scores very high around 1 pm, pointing towards a distinct effect of the changed timing.

At first glance, the results from the second day (second graph) is less optimistic, there is no sign of the peak around 1 pm. However, the observant reader will notice that there are no measurements recorded between approximately 11 am and 3 pm (shame on me…), meaning that the function in my fingers might very well have peaked during that time without me having recorded it.

Mental note to self: Make sure to record frequently, especially between 11 am and 3 pm.

The first day on the tweaked dose went OK, no fantastic change, but I didn’t expect that either. Let me try explaining in some more detail, how the different Parkinson’s medication works.

Remember the different types of Parkinson’s medication I mentioned yesterday?
Let’s call the levo-dopa based medication type A. Further, let’s call the kind that imitates the effects of dopamine type B. You might remember that there are two kinds of Parkinson’s medication that inhibits the transformation of dopamine into other chemicals. One type has no effect by itself, but only when taken at the same time as type A, we can call this kind of medication type C. And let’s call the last kind type D. All these different drugs behave differently in the body, they have different uptake rates and biological half-lives (this is where my background in chemical engineering comes very handy). And this, as you might realise, results in an extremely complicated system of different chemical reactions, that in an ideal situation would give me an even concentration of the substances lacking in my brain. Unfortunately, there is no easy way of measuring the concentration of these substances, so instead I try measuring the effect of these substances, meaning that I try to find ways to evaluate my different symptoms objectively, but more about the measurements in a later post.

As you can see, the regimen is in no way simple, but it has served me very well for the last few years. You might notice that my 11:30 dose consisted of only a type A and if you have been really paying attention, you might wonder why I don’t enhance the effect of the A with a C…. which is exactly what I have done. My “new” regimen is identical with the old one, save dose number 2 of the day. I now take it half an hour earlier and have added a type C. This might sound like a ridiculously small change, but I want to reduce the risk of getting unpleasant side effects. I use my iPhone, iPad and laptop to monitor the effect of the change. More about that later.

These last few days have made me even more aware of how extremely dependent I am of my medications, and if you’re reading this and have Parkinson’s yourself, this is probably very much old news. For people who have not experienced this, I completely understand that this is difficult to understand.
Let me quote an analogue that an experienced and very appreciated neurologist use to describe the process:

Currently, the ruling theory is that the wide range of symptoms falling under the Parkinson’s disease umbrella are caused by a lack of dopamine in the brain. Dopamine is one of a number of neurotransmitters, that together constitutes the signaling system within the brain. (I say currently, because there are theories that other neurotransmitters are also affected). However, the neurologist in question says that dopamine acts like the power steering (“servostyrning” in Swedish), i.e. making movements smoother and less effort-demanding. If the power steering fails, the car can still move and turn, but it takes a lot more effort to do so. For people with a dopamine deficiency, moving around, walking etc, takes a lot more energy when medication levels are low than when they are on a higher level.

Parkinson’s medication come in a few different varieties and these can be combined in a number of ways to achieve the best effect. Very simplified, these varieties are:
– medication based on levodopa, which, once it reaches the brain, is transformed into dopamine
– medication that mimic the effects of dopamine
– medication that inhibits the decomposition of dopamine in two different ways, hence leaving more of this precious chemical to our starving brains

My cocktail of Parkie-drugs consists of one of each of these four types, carefully combined in a collaboration with my neurologist, with whom I am fortunate enough to have developed true Shared Decision Making.

The change in medication is a very small change, barely more than a tweak, but I have learnt over the years, that medicating against Parkinson’s is like balancing a very thin line between wanted effects and unwelcome side effects. I also know that the resulting effect of a change will take weeks or even months to stabilise.